Actinic Keratosis (Hornlike Projection Known As Cutaneous Horn)
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ACTINIC KERATOSES DEFINITION Actinic keratoses (also known as solar keratosis) are rough, scaly erythematous patches or spots on the skin that develop on sun-damaged skin typically in elderly patients with lighter skin types from years of exposure to the sun. They are most commonly found on areas of skin typically exposed to the sun ( face, lips, ears, back of the hands, forearms, scalp or neck). Actinic keratoses enlarge slowly, take years to develop (usually first appearing in older adults) and usually cause no signs or symptoms other than the lesion on the skin. OVERVIEW Actinic keratoses (Ak) (also called "solar keratoses" and "senile keratoses") represent focal areas of abnormal keratinocyte proliferation and are considered premalignant lesions with low individual potential to malignant transformation (less than 1 in 1000 per annum) (pregression to squamous cell carcinoma - SCC) and a high spontaneous regression (in the order of 15-25% for Aks over 1-year period) Aks are often recognized by touch rather than sight. In fact Aks start out as small barely perceivable rough spots of skin that feel similar to rubbing sandpaper. The color ranges from skin-colored to pink to reddish brown. Most often, they appear as multiple discrete, flat or elevated, thickened, scaly or warty, keratotic lesions. Lesions typically have an erythematous base . They are usually 3-10 mm in diameter and grow slowly, usually without signs or symptoms but occasionally they may become pruritic or tender. They may enlarge into broader, more elevated hyperkeratotic plaques several centimetres in diameter. Occasionally, a lesion grows to resemble an animal horn and is called a “cutaneous horn (often referred has hypertrophic AK). Development of AKs may occur as early as the third or fourth decade of life in individuals who live in areas of high solar radiation, are fair-skinned with a history of extensive sun exposure, and do not use sunscreen for photoprotection. Usually, patients demonstrate a background of solar-damaged skin with telangiectasias, elastosis, and pigmented lentigines. 1 WHAT DOES AK MEAN? The two words “actinic” and “keratoses” precisely describe what has happened to the skin. “Actinic” comes from the Greek word for ray, “aktis,” and indicates that radiant energy (such as sunlight) has produced chemical changes. The word “keratoses” means the skin has become hard and callous. So AK literally means thickened scaly growth (keratosis) caused by sunlight (actinic). 2 WHAT DOES AK LOOK LIKE? While AKs, usually multiple, share common characteristics, such as being flat to slightly raised or thickened, dry or crusty, scaly or warty, rough patch or bump on sun-damaged skin. But not all AKs look alike. Some are skin-colored and may be easier to feel than see. These lesions often feel much like sandpaper. The base color may be light or dark, ranging from pink to red to brown, or a combination of these or the same color as skin. Each one can range from the size of a pinhead to 2-3 cm across. The top of each one may have a yellow-white crust. They feel rough and dry, and are slightly raised from the surface of the skin. Several solar keratoses may develop at about the same time, often in the same area of skin. Sometimes several join together and form a large flatish rough area of skin. Solar keratoses usually develop on areas of skin which have been exposed to the sun a lot. For example, on the face, neck, bald patches on the scalp, and the backs of the hands. They may appear in other areas in people who do a lot of sunbathing. There are usually no other symptoms. Rarely, may get an itchy, pricking or tender sensation from affected areas of skin. It can also become inflamed and surrounded by redness. In rare instances, actinic keratoses can bleed. Aks later grow into a tough, wart-like area. Sometimes AKs undergo rapid upward growth producing an exaggerated hyperkeratosis: a finger-like growth of hard skin, a horn-like projection above the skin surface appears to come out of a solar keratosis : it becomes a “cutaneous horn,” so named because it resembles the horn of an animal. The size of a cutaneous horn may range from that of a 3 pinhead to a pencil eraser, and the shape may be straight or curved. Sometimes skin cancer hides below a cutaneous horn. The skin around an AK tends to show evidence of sun damage, such as wrinkles and furrows (deep wrinkles). Clinically AK can be divided in three grades: • Grade I - easy visible, slightly palpable (feels better than seen) • Grade II - easily visible, palpable (easily felt and seen) • Grade III - frankly visible, hyperkeratotic (clinically obvious) The lesions begin as small, rough spots that are easier felt than seen with a sandpaperlike texture . With time, the lesions enlarge, usually becoming red and scaly. Most lesions are only 3-10 mm, but they may enlarge to several centimeters in size. Actinic keratoses may show the following variants: • Hyperkeratotic actinic keratosis (hornlike projection known as cutaneous horn) • Bowenoid actinic keratosis 4 • Pigmented actinic keratosis (also known as spreading pigmented AK, displays a variable color, ranging from brown to yellowish-black, with a smooth, verrucous or slightly scaly surface) 5 • Lichenoid (lichen planus-like) actinic keratosis (a pink papule or plaque, frequently located on the upper extremities and upper torso, and may be difficult to differentiate clinically from BCC). • Atrophic actinic keratosis (lacks the epidermal proliferation seen in the hypertrophic type) 6 Overlapping between subtypes may be observed. WHO GETS ACTINIC KERATOSES? Because long-term UV light exposure is implicated as the cause of Aks and AKs frequency correlates with cumulative UV exposure, AKs are more common in patients aged 50 years and older. The typical patient with AKs is an elderly, fair-skinned, sun-sensitive person. AKs occur almost exclusively in whites, especially those fair skin, redheaded or blond with blue, green or hazel eyes, who burn frequently and tan poorly. Because their skin has less protective pigment, they are the most susceptible to sunburn and other forms of sun damage. According with Fitzpatrick skin type, patients with AKs tend to have Fitzpatrick type I or II skin, which burns and does not tan. The prevalence is reduced in persons with Fitzpatrick types III, IV, and V skin and is nonexistent in those with Fitzpatrick type VI skin. Sensitivity to UV light is inherited. The incidence increases with each decade of life and is greater in residents of sunny countries closer to the equator. Men have a slightly increased frequency of AK. But AKs also affect individuals with a history of cumulative sun exposure, who have had increased sun exposure and higher-intensity exposure such as having worked outdoors for long periods or who work with substances that contain polycyclic aromatic hydrocarbons such as coal or tar. For exemple roofers that work with tar and outdoors. Sun-damaged skin is also dry, discoloured and wrinkled. Patients immunosuppressed following organ transplantation are at markedly increased risk of developing AKs just like people affected by albinism or xeroderma pigmentosum, whose skin is very sensitive to UV rays. 7 WHEN DOES AK APPEAR? As it usually takes years of sun exposure to develop an AK (because directly correlated to cumulative UV exposure), older people tend to be the most commonly affected. So likelihood of developing Ks increases with age, and lesions usually appears after age 50. But Aks may appear at a much earlier age in people who live in geographic areas with year-round high-intensity sunlight, who work outdoors, or who do a lot of sunbathing or use tanning beds and sun lamps. Development of actinic keratoses may occur as early as the third or fourth decade of life in patients who live in areas of high solar radiation, are fair-skinned, and do not use sunscreen for photoprotection. Summarizing, frequency increases with skin type, age (50 years and older), proximity to the equator, outdoor occupation, amount of sun damage. 8 WHY DOES AK APPEAR? Ak is a reflection of abnormal skin cell development due to exposure to chronic exposure to ultraviolet light (both UVB -290-320 nm and UVA -320-400 nm). While UV-A (320 - 400 nm) induced photo-oxidative stress indirectly induces characteristic DNA mutations, UV-B (290 - 320 nm) irradiation directly results in the formation of cyclobutane (thymin) dimer formation in DNA and RNA. If there are no appropriate repair mechanisms, these DNA changes are the starting phase of keratinocyte mutations which can progress into the development of AKs. UV radiations are not only the initiators but also the promoters. Other factors that can induce AKS are repeated iatrogenic exposure to UV-A, with or without combination with psoralenes, X-rays or radioisotopes. The skin is normally pretty good at repairing any minor damage. Indeed overexposure to UV in normal skin induces an intrinsic, highly complex programme of auto-orchestrated cell death (p53-dependent apoptosis), which serves to protect the skin from damaged cells. Histologically these individual apoptotic keratinocytes are often seen in the epidermis of skin overexposed to sunlight or UV radiation and are known as "sunburn" cells. But, over the years, some areas of skin are unable to cope with the repeated exposure to sun: UVs induce mutations of the tumor suppressor gene TP53 and basal keratinocytes with mutated TP53 may not respond normally to UV-induced apoptosis, allowing further proliferation and development of new genetic abnormalities. 9 Immunosuppression following solid organ transplantation may increase the risk for aktinic keratosis, but, only if there is sun exposure. So, it is not a recent bout of sun-tanning that causes them but repeated minor sun- damage to the skin over time: AK frequency correlates with cumulative UV exposure.